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Sacubitril/valsartan inverse remodeling - a prospective echocardiographic study

Session Poster Session 3

Speaker Geoffrey Bayard

Event : Heart Failure 2019

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure: Pharmacotherapy
  • Session type : Poster Session

Authors : G Bayard (Saint Etienne,FR), R Pierrard (Saint Etienne,FR), K Isaaz (Saint Etienne,FR), A Da Costa (Saint Etienne,FR)

G Bayard1 , R Pierrard1 , K Isaaz1 , A Da Costa1 , 1CHU Saint Etienne Hopital Nord, Cardiology - Saint Etienne - France ,


Background. Sacubitril/valsartan has been shown to improve mortality and reduce hospitalizations in patients with heart failure (HF) with reduced ejection fraction (HFrEF). Although the physiological action mechanisms of sacubitril/valsartan are well described, its effects on left ventricular (LV) remodelling and other echocardiographic (echo) parameters have not been prospectively studied. Objective. The aim of this prospective study was to: (1) evaluate if sacubitril/valsartan impacts LV remodelling based on echo parameters; (2) identify the predictive factors of sacubitril/valsartan response or intolerance. Methods. From May 2017 to September 2018, 52 HF patients were prospectively enrolled using Paradigm-HF criteria: Class II, III, or IV HF; ejection fraction (EF) of 40% or less; hospitalized for HF within the previous 12 months. Echo evaluation was performed before initiating sacubitril/valsartan and 3 months after optimal dose adjustment. Based on previous studies, patients with (absolute) improvement in left ventricular ejection fraction (LVEF) =5% were considered significant sacubitril/valsartan responders. Results. The 52 patients completing the study were characterized by age: 70±10 years; gender: 11 women; aetiology: idiopathic in 20 and ischaemic in 32; NYHA Class: II in 17 and III in 35; LVEF: 32±5%; NTProBNP: 1805±1914pg/mL. The final population comprised 41 pts (79%), as 11 (21%) did not tolerate sacubitril/valsartan therapy. Under sacubitril/valsartan, several echo parameters significantly improved: LVEF from 32.6±5 to 36±6% (p<0.0001); LVES volume from 117±40 to 108±46mL (p=0.0051; LVEDD from 60±4 to 57±5mm (p=0.0002); mean right ventricular systolic pressure (RVSP) from 39±10 to 32±8 (p=0.0001). No significant modifications were observed concerning LV diastolic parameters or RV echo parameters. Sacubitril/valsartan echo responders (n=18/41; 42%) had less severe LV remodelling, as shown by LVEDV: 144±37 vs. 193±47mL, p=0.0009; LVESV: 96±28 vs. 133±42mL; p=0.003; LVTDD: 61±4 vs. 57±5mm; p=0.02; significant mitral regurgitation: 6/18 (33%) vs. 16/23 (69%), p=0.02; no diastolic LV or RV parameters impacted sacubitril/valsartan response. Predictors of sacubitril/valsartan intolerance were baseline creatinine level: 137±99 vs. 100±24, p=0.03; LVEF: 29±6 vs. 33±5%; p=0.04. Conclusions. In HFrEF patients, sacubitril/valsartan significantly improves LV systolic remodelling, without any significant effects on LV diastolic or RV systolic echo parameters. Sacubitril/valsartan responders exhibit both less severe LV remodelling and less significant mitral regurgitation. Accordingly, sacubitril/valsartan could be used as soon as possible in HFrEF patients in order to limit LV remodelling, while precluding non-response or intolerance.

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